Tuesday, June 30, 2009
Documentary on Women's Sexual Health
If you are a woman who would be interested in taking part in an hour long documentary concerning women's sexual health issues please contact us at info@twshf.org.
Friday, June 26, 2009
TWSHF Expert-Dr Marjorie Green on Dr. Radio NYU June 29th Noon EST
Dr. Miriam Greene host of Sexual Health on SIRIUS Channel 114 & XM 119 will feature Dr. Marjorie Green, the Director of The Mount Auburn Menopause and Female Sexual Medicine Center, a Clinical Instructor with Harvard Medical School, and a TWSHF Expert at Noon EST June 29th.
This is a chance to have your sexual health questions answered by leading experts.
Call to ask questions at 1-877-698-3627/1-877-NYU-DOCS. Or email questions now to docs@sirius-radio.com.
This broadcast is powered by NYU Langone Medical Center. Doctor Radio is your chance to talk to dozens of respected doctors, plus special guest host physicians and medical experts from around the world.Hear Doctor Radio 24/7 on SIRIUS Ch. 114 & XM 119.
This is a chance to have your sexual health questions answered by leading experts.
Call to ask questions at 1-877-698-3627/1-877-NYU-DOCS. Or email questions now to docs@sirius-radio.com.
This broadcast is powered by NYU Langone Medical Center. Doctor Radio is your chance to talk to dozens of respected doctors, plus special guest host physicians and medical experts from around the world.Hear Doctor Radio 24/7 on SIRIUS Ch. 114 & XM 119.
Tuesday, June 16, 2009
New Scientific Finding-Stress Causes Sexual Dysfunction
New findings on how stress causes sexual dysfunction and infertility16. June 2009 02:49
University of California, Berkeley, researchers have found what they think is a critical and, until now, missing piece of the puzzle about how stress causes sexual dysfunction and infertility.
Scientists know that stress boosts levels of stress hormones - glucocorticoids such as cortisol - that inhibit the body's main sex hormone, gonadotropin releasing hormone (GnRH), and subsequently suppresses sperm count, ovulation and sexual activity.
The new research shows that stress also increases brain levels of a reproductive hormone named gonadotropin-inhibitory hormone, or GnIH, discovered nine years ago in birds and known to be present in humans and other mammals. This small protein hormone, a so-called RFamide-related peptide (RFRP), puts the brakes on reproduction by directly inhibiting GnRH.
The common thread appears to be the glucocorticoid stress hormones, which not only suppress GnRH but boost the suppressor GnIH - a double whammy for the reproductive system.
"We know stress affects the top-tier reproductive hormone, GnRH, but we show, in fact, that stress also affects another high-level hormone, GnIH, to cause reproductive dysfunction," said lead author Elizabeth Kirby, a graduate student at UC Berkeley's Helen Wills Neuroscience Institute. "This work provides a new target for researchers, a new way to think about infertility and dysfunction. The more we know, the more we can look for ways to treat it."
The results will be published the week of June 15 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS)
The conclusions are based on experiments in rats and inferences from the effects of the hormone in birds. But if this new reproductive hormone acts the same way in all mammals, researchers say the finding could not only change the way physicians look at human reproductive problems, but also affect how breeders approach animal husbandry and captive breeding programs for endangered species.
"There is a growing body of work that points to GnIH as being a big player in the inhibition of reproduction in mammals," said co-author George Bentley, UC Berkeley assistant professor of integrative biology. "We didn't have any hint of this stress effect nine years ago, when GnIH was first discovered."
In humans, chronic stress can lead to a drop in sex drive as well as a drop in fertility. Even the stress of infertility treatments can block their effectiveness, as evidenced by many anecdotes about couples conceiving children after the failure of assisted reproduction.
Animal breeding also is affected by stress. Zoos, in particular, have difficulty getting some animals to reproduce in captivity, Bentley said.
Based on animal experiments, researchers attribute much of this stress effect on sexual function to an increase in glucocorticoids - stress hormones - produced by the adrenal gland. In the brain, these glucocorticoids suppress the main reproductive hormone, GnRH, which in turn causes a shut-down of the release of the gonadotropins luteinizing hormone and follicle-stimulating hormone by the pituitary, and then a suppression of testosterone, estradiol and sexual behavior.
In 2000, however, a new reproductive hormone was discovered in birds and dubbed gonadotropin-inhibitory hormone (GnIH) because it had the opposite effect of GnRH - it inhibited release of gonadotropins, thereby suppressing reproduction.
"It's very adaptive to not be wasting resources on reproduction during times of acute stress, to just shut down reproduction for 24 hours or so until the stress is gone," said co-author Daniela Kaufer, a UC Berkeley assistant professor of integrative biology who looks at how stress affects molecular processes in the brain. "These functions go back in evolution a long way."
Because of the negative effects of GnIH on reproduction, Bentley, who helped establish the critical role played by GnIH in birds, teamed up with Kaufer and Kirby to explore whether stress might affect GnIH levels in the brain. The homologous hormones in mammals have been dubbed RFamide-related peptides, or RFRPs.
Kirby showed that acutely stressed rats showed increased RFRP levels for several hours, but that levels returned to normal by the next day. Chronically stressed rats, however, were left with longer-term elevations of RFRP levels in the dorsomedial hypothalamus area of the brain, and suppression of activity in the reproductive axis - the hypothalamus-pituitary-gonadal hormone cascade - that is associated with lowered sexual activity.
"With chronic stress, glucocorticoids went sky high," Kirby said.
To determine the role of glucocorticoids, Kirby removed the adrenal glands of male rats, eliminating the source of the hormone. Without adrenals, stress no longer affected RFRP levels in the brain. The researchers also showed that the cells that produce RFRP have receptors for glucocorticoids, a clear indication that these stress hormones can directly affect the cells that produce RFRP.
"Critically, we show that RFRP neurons express the receptors for glucocorticoids, which are released from the adrenal glands in response to stress, and that removal of the adrenal glands prevents the stress-induced, up-regulation of RFRP," Bentley said. "Thus, we believe we have identified an entirely novel pathway for stress-induced reproductive dysfunction."
Kirby noted that adrenal hormones are critical to survival, so removing the gland and thus glucocorticoids is not a solution to chronic stress.
However, Kaufer said, it may be possible to block GnIH to reduce some of the effects of stress on reproduction.
The researchers plan to confirm the results in female rats and investigate further the role of GnIH in reproduction.
http://www.berkeley.edu/
University of California, Berkeley, researchers have found what they think is a critical and, until now, missing piece of the puzzle about how stress causes sexual dysfunction and infertility.
Scientists know that stress boosts levels of stress hormones - glucocorticoids such as cortisol - that inhibit the body's main sex hormone, gonadotropin releasing hormone (GnRH), and subsequently suppresses sperm count, ovulation and sexual activity.
The new research shows that stress also increases brain levels of a reproductive hormone named gonadotropin-inhibitory hormone, or GnIH, discovered nine years ago in birds and known to be present in humans and other mammals. This small protein hormone, a so-called RFamide-related peptide (RFRP), puts the brakes on reproduction by directly inhibiting GnRH.
The common thread appears to be the glucocorticoid stress hormones, which not only suppress GnRH but boost the suppressor GnIH - a double whammy for the reproductive system.
"We know stress affects the top-tier reproductive hormone, GnRH, but we show, in fact, that stress also affects another high-level hormone, GnIH, to cause reproductive dysfunction," said lead author Elizabeth Kirby, a graduate student at UC Berkeley's Helen Wills Neuroscience Institute. "This work provides a new target for researchers, a new way to think about infertility and dysfunction. The more we know, the more we can look for ways to treat it."
The results will be published the week of June 15 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS)
The conclusions are based on experiments in rats and inferences from the effects of the hormone in birds. But if this new reproductive hormone acts the same way in all mammals, researchers say the finding could not only change the way physicians look at human reproductive problems, but also affect how breeders approach animal husbandry and captive breeding programs for endangered species.
"There is a growing body of work that points to GnIH as being a big player in the inhibition of reproduction in mammals," said co-author George Bentley, UC Berkeley assistant professor of integrative biology. "We didn't have any hint of this stress effect nine years ago, when GnIH was first discovered."
In humans, chronic stress can lead to a drop in sex drive as well as a drop in fertility. Even the stress of infertility treatments can block their effectiveness, as evidenced by many anecdotes about couples conceiving children after the failure of assisted reproduction.
Animal breeding also is affected by stress. Zoos, in particular, have difficulty getting some animals to reproduce in captivity, Bentley said.
Based on animal experiments, researchers attribute much of this stress effect on sexual function to an increase in glucocorticoids - stress hormones - produced by the adrenal gland. In the brain, these glucocorticoids suppress the main reproductive hormone, GnRH, which in turn causes a shut-down of the release of the gonadotropins luteinizing hormone and follicle-stimulating hormone by the pituitary, and then a suppression of testosterone, estradiol and sexual behavior.
In 2000, however, a new reproductive hormone was discovered in birds and dubbed gonadotropin-inhibitory hormone (GnIH) because it had the opposite effect of GnRH - it inhibited release of gonadotropins, thereby suppressing reproduction.
"It's very adaptive to not be wasting resources on reproduction during times of acute stress, to just shut down reproduction for 24 hours or so until the stress is gone," said co-author Daniela Kaufer, a UC Berkeley assistant professor of integrative biology who looks at how stress affects molecular processes in the brain. "These functions go back in evolution a long way."
Because of the negative effects of GnIH on reproduction, Bentley, who helped establish the critical role played by GnIH in birds, teamed up with Kaufer and Kirby to explore whether stress might affect GnIH levels in the brain. The homologous hormones in mammals have been dubbed RFamide-related peptides, or RFRPs.
Kirby showed that acutely stressed rats showed increased RFRP levels for several hours, but that levels returned to normal by the next day. Chronically stressed rats, however, were left with longer-term elevations of RFRP levels in the dorsomedial hypothalamus area of the brain, and suppression of activity in the reproductive axis - the hypothalamus-pituitary-gonadal hormone cascade - that is associated with lowered sexual activity.
"With chronic stress, glucocorticoids went sky high," Kirby said.
To determine the role of glucocorticoids, Kirby removed the adrenal glands of male rats, eliminating the source of the hormone. Without adrenals, stress no longer affected RFRP levels in the brain. The researchers also showed that the cells that produce RFRP have receptors for glucocorticoids, a clear indication that these stress hormones can directly affect the cells that produce RFRP.
"Critically, we show that RFRP neurons express the receptors for glucocorticoids, which are released from the adrenal glands in response to stress, and that removal of the adrenal glands prevents the stress-induced, up-regulation of RFRP," Bentley said. "Thus, we believe we have identified an entirely novel pathway for stress-induced reproductive dysfunction."
Kirby noted that adrenal hormones are critical to survival, so removing the gland and thus glucocorticoids is not a solution to chronic stress.
However, Kaufer said, it may be possible to block GnIH to reduce some of the effects of stress on reproduction.
The researchers plan to confirm the results in female rats and investigate further the role of GnIH in reproduction.
http://www.berkeley.edu/
Friday, May 29, 2009
Listen to TWSHF Experts & A Survivor On Breast Cancer & Sexuality
Listen to TWSHF experts and a breast cancer survivor discuss cancer's impact on intimacy and sexuality on Blog Talk Radio with Kelley Connors.
Learn that many of the treatments for cancer can cause vaginal dryness and pain. Plus, women may loose desire for intimacy not only because of body image concerns, but also because of chemotherapy and even tamoxifen.
Our breast cancer survivor, Nancy Singleton, is a patient navigator with WAR or Women at Risk. Women At Risk (WAR®)is the Breast Cancer Program at NewYork-Presbyterian Hospital/Columbia University Medical Center, whose mission is to enhance the lives of women who are at high risk for the development of breast cancer and women with breast cancer through research, education and support.
Click on the program above to learn more.
Listen to Learn that many of the treatments for cancer can cause vaginal dryness and pain. Plus, women may loose desire for intimacy not only because of body image concerns, but also because of chemotherapy and even tamoxifen.
Our breast cancer survivor, Nancy Singleton, is a patient navigator with WAR or Women at Risk. Women At Risk (WAR®)is the Breast Cancer Program at NewYork-Presbyterian Hospital/Columbia University Medical Center, whose mission is to enhance the lives of women who are at high risk for the development of breast cancer and women with breast cancer through research, education and support.
Click on the program above to learn more.
Tuesday, May 26, 2009
Does spontaneous genital tract trauma impact postpartum sexual function?
Rogers RG, Borders N, Leeman LM, Albers LL.
MidwiferyDivision, Department of Obstetrics and Gynecology, 1 University ofNew Mexico, MSC10 5580, Albuquerque, NM 87131-0001, USA.
Changes in sexual function are common in postpartum women. In this comparative, descriptive study, a prospective cohort of midwifery patients consented to documentation of genital trauma at birth and assessment of sexual function at 3 months postpartum. The impact of spontaneous genital trauma on postpartum sexual function was the focus of the study. Trauma was categorized into minor trauma (no trauma or first-degree perineal or other trauma that was not sutured) or major trauma (second-, third-, or fourth-degree lacerations or any trauma that required suturing). Women who underwent episiotomy or operative delivery were excluded. Fifty-eight percent (326/565) of enrolled women gave sexual function data; of those, 276 (85%) reported sexual activity since delivery. Seventy percent (193) of women sustained minor trauma and 30% (83) sustained major trauma. Sexually active women completed the Intimate Relationship Scale (IRS), a 12-item questionnaire validated as a measure of postpartum sexual function. Both trauma groups were equally likely to be sexually active. Total IRS scores did not differ between trauma groups nor did complaints of dyspareunia. However, for two items, significant differences were demonstrated: women with major trauma reported less desire to be held, touched, and stroked by their partner than women with minor trauma, and women who required perineal suturing reported lower IRS scores than women who did not require suturing.
J Midwifery Womens Health. 2009 Mar-Apr;54(2):98-103
MidwiferyDivision, Department of Obstetrics and Gynecology, 1 University ofNew Mexico, MSC10 5580, Albuquerque, NM 87131-0001, USA.
Changes in sexual function are common in postpartum women. In this comparative, descriptive study, a prospective cohort of midwifery patients consented to documentation of genital trauma at birth and assessment of sexual function at 3 months postpartum. The impact of spontaneous genital trauma on postpartum sexual function was the focus of the study. Trauma was categorized into minor trauma (no trauma or first-degree perineal or other trauma that was not sutured) or major trauma (second-, third-, or fourth-degree lacerations or any trauma that required suturing). Women who underwent episiotomy or operative delivery were excluded. Fifty-eight percent (326/565) of enrolled women gave sexual function data; of those, 276 (85%) reported sexual activity since delivery. Seventy percent (193) of women sustained minor trauma and 30% (83) sustained major trauma. Sexually active women completed the Intimate Relationship Scale (IRS), a 12-item questionnaire validated as a measure of postpartum sexual function. Both trauma groups were equally likely to be sexually active. Total IRS scores did not differ between trauma groups nor did complaints of dyspareunia. However, for two items, significant differences were demonstrated: women with major trauma reported less desire to be held, touched, and stroked by their partner than women with minor trauma, and women who required perineal suturing reported lower IRS scores than women who did not require suturing.
J Midwifery Womens Health. 2009 Mar-Apr;54(2):98-103
Thursday, April 30, 2009
Guest Blogger: Women’s Secrets, men’s Muscles Unveiled
By Harold Schulman, MD
What does a semi-retired male gynecologist do? He does odd jobs, but if he was a professor and teacher he might write a book dealing with male and female sexuality.
That’s what I did. Why? Women have taught me about their dissatisfaction with their doctors, particularly in the area of sexuality. Furthermore since I had the time, I felt I wanted to share what I learned with doctors, health workers and people about the cultural influences surrounding women and men. These issues are rarely touched upon in residency programs, and I was surprised to learn how much I didn’t know. It was a nature-nurture issue to me.
For many years as a residency program director, I established a yearly course on sexuality for the residency staff. There were resources available but the emergence of porno videos destroyed the course and the need or value of its teachers.
As a practitioner, I was disappointed when I saw how many gynecologists were uncomfortable with these issues. The doctors frequently gave advice that was appalling. I was interested and comfortable and utilized the resources that were available including Sinclair Institute resources.
Thus, I wrote a book, recently published. The title, Women’s Secrets, men’s Muscles Unveiled is a not so veiled effort to attract men and women.
My initial motivation came from the Vagina Monologue, and my discovery of the word, yoni from the Camphausens. I felt that there should be dialogues, not monologues to enhance relationships between men and women. I have no experience with unisexual unions.
For the next five years I ploughed the Internet to find answers and thoughts that were new to me. My life long history in the arts enabled me to integrate art, and literature into my dialogue. My confusion about faith and religion drew me to spiritual thoughts that were intertwined. I found a publisher, iUniverse.com, that gave me enormous support on how to write for the public.
I would love to hear from and share ideas with members of TWSHF.
I f I have stimulated your curiosity see my web site and blog at http://web.mac.com/haroldschulmanmd%20or%20Amazon.com.
Harold Schulman, MD
What does a semi-retired male gynecologist do? He does odd jobs, but if he was a professor and teacher he might write a book dealing with male and female sexuality.
That’s what I did. Why? Women have taught me about their dissatisfaction with their doctors, particularly in the area of sexuality. Furthermore since I had the time, I felt I wanted to share what I learned with doctors, health workers and people about the cultural influences surrounding women and men. These issues are rarely touched upon in residency programs, and I was surprised to learn how much I didn’t know. It was a nature-nurture issue to me.
For many years as a residency program director, I established a yearly course on sexuality for the residency staff. There were resources available but the emergence of porno videos destroyed the course and the need or value of its teachers.
As a practitioner, I was disappointed when I saw how many gynecologists were uncomfortable with these issues. The doctors frequently gave advice that was appalling. I was interested and comfortable and utilized the resources that were available including Sinclair Institute resources.
Thus, I wrote a book, recently published. The title, Women’s Secrets, men’s Muscles Unveiled is a not so veiled effort to attract men and women.
My initial motivation came from the Vagina Monologue, and my discovery of the word, yoni from the Camphausens. I felt that there should be dialogues, not monologues to enhance relationships between men and women. I have no experience with unisexual unions.
For the next five years I ploughed the Internet to find answers and thoughts that were new to me. My life long history in the arts enabled me to integrate art, and literature into my dialogue. My confusion about faith and religion drew me to spiritual thoughts that were intertwined. I found a publisher, iUniverse.com, that gave me enormous support on how to write for the public.
I would love to hear from and share ideas with members of TWSHF.
I f I have stimulated your curiosity see my web site and blog at http://web.mac.com/haroldschulmanmd%20or%20Amazon.com.
Harold Schulman, MD
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